Assessments of Oxygenation

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Chapter 4 Assessments of Oxygenation

Asheesh Kumar, MD , Michael E. Canham, MD , Ulrich H. Schmidt, MD, PhD

1 What do arterial blood gas (ABG) instruments measure?

The current ABG instruments measure pH, PCO₂, and PO₂ using three separate electrodes. The blood gas samples are placed through an inlet into a temperature-controlled chamber (usually 37° C) where the blood is exposed to these three electrode tips. Newer ABG machines have simultaneous CO-oximeter measurements as well. Consequently, with use of an absorption spectrophotometer, measurements of reduced hemoglobin, oxyhemoglobin, carboxyhemoglobin, and methemoglobin can also be made. Often, hemoglobin and basic electrolytes can be measured simultaneously.

2 When should ABGs be used?

Analysis of ABGs is used extensively in the critical care setting to evaluate both acid-base status and oxygen and carbon dioxide gas exchange. Analysis of ABGs can be useful in virtually any critical care situation, especially with regard to the acid-base status, adequacy of perfusion, and adequacy of gas exchange.

3 What alternatives exist to measure respiratory gases and gas exchange?

ABGs, specifically acid-base status, are useful for evaluation of systemic pH, especially in the setting of significant metabolic acidoses. However, alternative mechanisms are clinically available to measure systemic oxygen and carbon dioxide levels.

Pulse oximetry: Pulse oximetry is a noninvasive, continuous method of measuring the saturation of hemoglobin by using the differential absorption of different wavelengths of light depending on the loading conditions of oxygen that can significantly reduce the number of ABGs measured in critically ill patients. Further, recent studies have validated the use of respiratory variation in pulse oximetry to detect fluid responsiveness in critically ill patients.

End-tidal carbon dioxide: In patients without significant pulmonary pathologic conditions, an end-tidal carbon dioxide monitor can approximate the plasma levels of carbon dioxide, indicating ongoing metabolic production and adequacy of ventilation.

Bicarbonate: Levels of serum bicarbonate can provide guidance about serum levels of carbon dioxide and pH, especially in the chronic setting. Elevations of serum bicarbonate can indicate chronic retention of carbon dioxide.

Exhaled carbon dioxide: The content of exhaled carbon dioxide over a given period of time can be measured by several commercially available devices. This can provide information regarding total body carbon dioxide production, as well as the adequacy of carbon dioxide elimination. Specifically, with use of the Bohr equation, the dead-space fraction can be calculated to assess the adequacy of ventilation and underlying degrees of pulmonary pathologic conditions.

Calculated minute ventilation: The overall minute ventilation can be calculated by multiplying the tidal volume by respiratory rate. Again, the minute ventilation can provide information about metabolic demands and production.

4 What is the alveolar gas equation?

The alveolar gas equation is a formula used to approximate the partial pressure of oxygen in the alveolus (PAO₂).

where PB is the barometric pressure, PH₂O is the water vapor pressure (usually 47 mm Hg), FiO₂ is the fractional concentration of inspired oxygen, and R is the gas exchange ratio. (The rate of CO₂ production to O₂ utilization is usually approximately 0.8 at rest). For example, at sea level:

As demonstrated by the alveolar gas equation, significant alterations of other values can affect the alveolar oxygen level. For example, significant elevation of plasma carbon dioxide can lead to a decrease in the partial pressure of alveolar oxygen. Further, changes in the respiratory quotient (e.g., supplemental nutrition with high carbohydrate content) can further decrease alveolar oxygenation because of a high CO₂ production–to–O₂ utilization ratio.

5 What is the alveolar-arterial PO₂ difference, or A − a gradient (A − aO₂ gradient)?

After calculation of the PAO₂ from the alveolar gas equation, the A − aO₂ gradient can be obtained by subtracting the PaO₂ measured from the ABG. The alveolar-to-arterial (A − aO₂) oxygen gradient is the difference between the amount of the oxygen in the alveoli (PAO₂) and the amount of oxygen dissolved in the plasma (PaO₂), as measured by ABG. For example, at sea level (with PCO₂ − 40, PO₂ − 92):

The normal A − aO₂ gradient is dependent on age, body position, and nutritional status. A normal A − a gradient for a young adult nonsmoker breathing air is between 5 and 10 mm Hg. Normally, the A − a gradient increases with age. For every decade a person has lived, his or her A − a gradient is expected to increase by 1 mm Hg. The A − aO₂ gradient is widened under normal conditions by age, obesity, fasting, supine position, and heavy exercise. One predictive equation for estimating PO₂ (at PB = 760 mm Hg) in relation to age is as follows: PO₂ = 109 − 0.43 × Age (in years).

6 How is the A − aO₂ gradient useful? What can cause significant elevations of the A − aO₂ gradient?

The A − aO₂ gradient may be affected by significant cardiopulmonary conditions that result in hypoxemia and/or hypocarbia. However, it must be noted that the A − a gradient normally increases with higher FiO₂, resulting in an elevated gradient without clinical hypoxemia. When receiving a high FiO₂, both PAO₂ and PaO₂ can increase. However, the PAO₂ increases disproportionately, causing the A − a gradient to increase. In one series, the A − a gradient in men breathing air and 100% oxygen varied from 8 to 82 mm Hg in patients younger than 40 years of age and from 3 to 120 mm Hg in patients older than 40 years of age.

Clinically significant hypoxemia associated with a widened A − aO₂ gradient is commonly due to:

V/Q mismatch: The normal heterogeneity of V/Q matching in the lung can be significantly altered by many disease states, resulting in a widened A − aO₂ gradient and clinical hypoxemia. Commonly, this can be seen with atelectasis, pneumonia, aspiration, pulmonary edema, and/or acute lung injury or adult respiratory distress syndrome (ARDS).

Right-to-left shunt: A right-to-left shunt exists when blood passes from the right to the left side of the heart without being oxygenated. Numerous anatomic shunts exist physiologically that contribute to the normal A − aO₂ gradient, such as the bronchial and thebesian circulation. Pathologic shunts can develop when nonventilated alveoli are perfused (atelectasis, pneumonia, edema, ARDS, pulmonary fibrosis).

Diffusion impairment: Diffusion impairment occurs when a limitation exists to the movement of oxygen from the alveoli into the pulmonary vasculature. This can be due to overall destruction of lung parenchyma, such as severe emphysema, or pathologic changes in the air-blood interface in the lung, such as fibrosis.

7 What clinical conditions can present with a normal A − aO₂ gradient?

Conditions that purely lower the alveolar concentration of oxygen without concomitant pulmonary pathologic conditions can result in clinically significant hypoxemia with a normal A − aO₂ gradient. Because many can result in complicating factors that cause significant elevations of the A − aO₂ gradient, such as atelectasis, consolidation, or aspiration events, these conditions are clinically rarely seen in isolation. Clinical hypoxemia with a normal A − aO₂ gradient occurs in the setting of low inspired partial pressure of oxygen (PiO₂). On the basis of the alveolar gas equation, this results from multiple factors.

Low FiO₂: This can be seen in a variety of clinical situations, such as hypoxic mixtures of inhaled gases. These are also readily correctable by administration of higher concentrations of oxygen; failure to respond to such therapy should prompt investigation of other causes of hypoxemia.

Low PB: Atmospheric pressure at sea level is approximately 760 mm Hg. As altitude increases, PB decreases; with significant elevations of altitude, low alveolar oxygen levels can develop. The mean measured PAO₂ measured at 8400 m (descent from summit of Mount Everest) above sea level was 30 mm Hg with an A − aO₂ gradient of 5.41 mm Hg.

Significant hypercarbia (elevated PaCO₂): Elevations of arterial carbon dioxide levels can result in decreases in alveolar oxygen levels. Pure hypercarbia is often the result of hypoventilation syndromes. These can be related to multiple factors:

Central nervous system (CNS) depression, such as drug overdose, structural CNS lesions, or ischemic CNS lesions that affect the respiratory center

Obesity hypoventilation (Pickwickian) syndrome

Impaired neural conduction, such as amyotrophic lateral sclerosis, Guillain-Barré syndrome, high cervical spine injury, or phrenic nerve paralysis

Muscular weakness, such as myasthenia gravis, muscular dystrophy, or residual neuromuscular blockade

Poor chest wall elasticity, such as a flail chest or kyphoscoliosis

8 What are point-of-care (POC) ABGs?

Current technology allows measurement of ABGs at the bedside with handheld blood gas analysis devices that use disposable cartridges. Several commercially available devices provide different test options to measure in addition to routine ABG values. Consequently, the reliability of each measured parameter may differ from one device to another.

9 How do POC ABGs work? What are their advantages and disadvantages?

The heparinized ABG specimen is placed into the POC cartridge, where the blood flows to different sites-sensors for analysis. The pH and PCO₂ are measured by direct potentiometry, and the PO₂ is measured amperometrically. The values for HCO₃, total CO₂, base excess, and oxygen saturation are calculated. POC testing can be performed by nurses, physicians, and respiratory therapists, and the ABG results are obtained more rapidly and may influence critical decisions. The major disadvantages include cost per cartridge, lack of preanalysis calibrations to ensure accuracy, and a lack of CO-oximetry measurements.

10 Given that oximetry is so readily available, painless, and accurate, why is ABG analysis necessary?

Oximetry and the newer technology that made it more accessible, affordable, and accurate have decreased the need for ABG analysis in monitoring oxygen saturation. In fact, the number of ABGs done has decreased with the influx of oximeters into virtually every department in a hospital. However, relying on oximetry alone can lead to misdiagnosis, increased cost, and potentially fatal respiratory arrest. Common clinical scenarios include

Hypercarbia: An increased PCO₂ from hypoventilation (e.g., in a patient receiving narcotics) can often be missed by a reassuring oxygen saturation. Although the pulse oximeter provides information regarding systemic oxygenation, it cannot provide data regarding systemic conditions of carbon dioxide. An ABG or venous blood gas measurement is necessary for further evaluation, because oxygenation can be maintained despite rising PCO₂ and impending respiratory failure.

Carbon monoxide (CO): CO diffuses rapidly across the pulmonary capillary membrane and binds to hemoglobin with approximately 240 times the affinity of oxygen. Standard pulse oximetry cannot screen for CO exposure, because it cannot differentiate carboxyhemoglobin from oxyhemoglobin, inasmuch as they absorb the same emitted light wavelength. Arterial blood gas measurements tend to be normal because PO₂ reflects oxygen dissolved in blood, and this process is not affected by CO. Acute CO poisoning must be clinically suspected on the basis of a suggestive history and associated physical examination findings (e.g., singed nasal hair, soot); specialized eight-wavelength pulse oximeters and ABG analysis with CO-oximetry are required to detect systemic CO.

Abnormal hemoglobin or hemoglobin variants: Methemoglobin is an altered state of hemoglobin in which the ferrous (Fe^2 +) irons of heme are oxidized to the ferric (Fe^3 +) state, which are unable to bind oxygen. In addition, the oxygen affinity of any remaining ferrous hemes is increased, resulting in a leftward shift of the oxygen dissociation curve. Large amounts of methemoglobin production can be induced by various drugs, including antibiotics and local anesthetics, such as benzocaine (commonly used for oropharyngeal topicalization). Methemoglobinemia may be clinically suspected by the presence of clinical cyanosis in the presence of a normal arterial PO₂ as obtained by ABGs. Classically, oxygen saturation as measured by pulse oximetry drops to 85%, as methemoglobin absorbs both wavelengths of light (660 and 940 nm) emitted by pulse oximetry resulting in an average value regardless of the true percentage of oxyhemoglobin.

Key Points Assessments of oxygenation

1. Multiple reliable methods are available for monitoring the adequacy of gas exchange in the critical care setting.

2. The ABG and the alveolar gas equation can be used to evaluate the mechanisms of hypoxemia in critically ill patients.

1 Barton C.W. Correlation of end-tidal CO₂ measurements to arterial PaCO₂ in non-intubated patients. Ann Emerg Med. 1994;23:562–563.

2 Durbin C.G., Rostow S.K. More reliable oximetry reduces the frequency of arterial blood gas analyses and hastens weaning after cardiac surgery: a prospective, randomized trial of the clinical impact of a new technology. Crit Care Med. 2002;30:1735–1740.

3 Feissel M., Teboul J.L., Merlani P., et al. Plethysmographic dynamic indices predict fluid responsiveness in septic ventilated patients. Intensive Care Med. 2007;33:993–999.

4 Fu E.S., Downs J.B., Schweiger J.W., et al. Supplemental oxygen impairs detection of hypoventilation by pulse oximetry. Chest. 2004;126:1552–1558.

5 Hampson N.B. Pulse oximetry in severe carbon monoxide poisoning. Chest. 1998;114:1036–1041.

6 Hess D., Schlottag A., Levin B., et al. An evaluation of the usefulness of end-tidal PCO₂ to aid weaning from mechanical ventilation following cardiac surgery. Respir Care. 1991;36:837–843.

7 Michael P.W., Grocott M.B., Martin D.S., et al. Arterial blood gases and oxygen content in climbers on Mount Everest. N Engl J Med. 2009;360:140–149.

8 Mithoefer J.C., Bossman O.G., Thibeault D.W., et al. The clinical estimation of alveolar ventilation. Am Rev Respir Dis. 1968;98:868–871.

9 Nuckton T.J., Alonso J.A., Kallet R.H., et al. Pulmonary dead-space fraction as a risk factor for death in the acute respiratory distress syndrome. N Engl J Med. 2002;346:1281–1286.

10 Perkins G.D., McAuley D.F., Giles S., et al. Do changes in pulse oximeter oxygen saturation predict equivalent changes in arterial oxygen saturation? Crit Care. 2003;7:R67.

11 Rodríguez-Roisin R., Roca J. Mechanisms of hypoxemia. Intensive Care Med. 2005;31:1017–1019.

12 Severinghaus J.W., Astraup P., Murray J.F. Blood gas analysis and critical care medicine. Am J Respir Crit Care Med. 1998;157:S114–S122.

13 Siddiki H., Kojicic M., Li G., et al. Bedside quantification of dead-space fraction using routine clinical data in patients with acute lung injury: secondary analysis of two prospective trials. Crit Care. 2010;14:R141.

14 Story D.A. Alveolar oxygen partial pressure, alveolar carbon dioxide partial pressure, and the alveolar gas equation. Anesthesiology. 1996;84:101.

15 Tobin M.J. Respiratory monitoring in the intensive care unit. Am Rev Respir Dis. 1988;138:1625–1642.

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